Aging is characterized by molecular damages that affects lipids, proteins and nucleic acids. These damages accumulate over time impairing several molecular functions, eventually leading to reduced physiological performance with an increase in disease risk and mortality. Untangling the chain of cause and consequences that eventually lead to physiological impairments has been, up to now, complicated. Many molecular changes start early in adult life and are progressive, so that there is not one single phenomenon that precedes later age-related changes.
In the last few decades molecular and genetic studies on aging have relied on canonical model organisms (i.e. the organisms of choice in biomedical research), namely yeast, nematode worms, fruit flies and – to a more limited extent - the mouse. These systems have allowed systematic investigations that provided fundamental conceptual advances.
More recently, the introduction of high-throughput technologies has facilitated genome sequencing, and non-canonical animal models, specifically selected for their exceptional life history, have entered in the aging arena.
Investigations of organisms of different physiology and phylogenetic relationships can certainly offer new study perspectives and interesting insights/cues for the understanding of many aging processes that remain uninvestigated and/or unexplained. In particular, animals that show either an exceptionally short lifespan (for example the turquoise killifish) or exceptional longevity (for example the naked mole rat) have been widely explored in recent times.
In this collection we welcome reviews and original research papers that make use of - or discuss the use of - non-standard model organisms for cellular aging research, including:
• Epigenetics of aging
• Cellular senescence
• Protein aggregation
• Neurodegeneration
• DNA damage
• Somatic mutations
• Telomere erosion
Contributions employing -omics approaches (comparative genomics, transcriptomics, and proteomics) are welcome, in addition to research using classical biochemical, molecular and cellular approaches.
Our ultimate aim is to provide the scientific community with the most updated and in-depth picture of comparative approaches to understanding aging.
Aging is characterized by molecular damages that affects lipids, proteins and nucleic acids. These damages accumulate over time impairing several molecular functions, eventually leading to reduced physiological performance with an increase in disease risk and mortality. Untangling the chain of cause and consequences that eventually lead to physiological impairments has been, up to now, complicated. Many molecular changes start early in adult life and are progressive, so that there is not one single phenomenon that precedes later age-related changes.
In the last few decades molecular and genetic studies on aging have relied on canonical model organisms (i.e. the organisms of choice in biomedical research), namely yeast, nematode worms, fruit flies and – to a more limited extent - the mouse. These systems have allowed systematic investigations that provided fundamental conceptual advances.
More recently, the introduction of high-throughput technologies has facilitated genome sequencing, and non-canonical animal models, specifically selected for their exceptional life history, have entered in the aging arena.
Investigations of organisms of different physiology and phylogenetic relationships can certainly offer new study perspectives and interesting insights/cues for the understanding of many aging processes that remain uninvestigated and/or unexplained. In particular, animals that show either an exceptionally short lifespan (for example the turquoise killifish) or exceptional longevity (for example the naked mole rat) have been widely explored in recent times.
In this collection we welcome reviews and original research papers that make use of - or discuss the use of - non-standard model organisms for cellular aging research, including:
• Epigenetics of aging
• Cellular senescence
• Protein aggregation
• Neurodegeneration
• DNA damage
• Somatic mutations
• Telomere erosion
Contributions employing -omics approaches (comparative genomics, transcriptomics, and proteomics) are welcome, in addition to research using classical biochemical, molecular and cellular approaches.
Our ultimate aim is to provide the scientific community with the most updated and in-depth picture of comparative approaches to understanding aging.
